Evidence map›Paper›PMID 40062767›Full record

ArticleAddiction biology2025

Treadmill Exercise Training Ameliorates Apoptotic Cells and DNA Oxidation in the Cerebral Cortex of Rats Exposed to Chronic Ketamine Abuse.

Salar Sabziparvar, Kazem Khodaei, Javad Tolouei Azar

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Article in Addiction biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Salar SabziparvarSport Physiology and Corrective Exercises Department, Sport Sciences Faculty, Urmia University, Urmia, Iran.ORCID 0009-0001-4604-8857
Kazem KhodaeiSport Physiology and Corrective Exercises Department, Sport Sciences Faculty, Urmia University, Urmia, Iran.ORCID 0000-0003-1566-2851
Javad Tolouei AzarSport Physiology and Corrective Exercises Department, Sport Sciences Faculty, Urmia University, Urmia, Iran.ORCID 0000-0002-2724-8474

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKetamine abuse damages brain function and structure, increasing reactive oxygen species and apoptosis in the cerebral cortex, but moderate-intensity continuous training (MICT) can enhance antioxidant defences and reduce apoptosis. Therefore, we aimed to answer whether MICT can reduce the side effects of chronic ketamine abuse.

method24 Wistar rats were split into control (CON), ketamine abuse (KET), exercise after ketamine withdrawal (KET + EX), and non-intervention ketamine withdrawal (KET + WD) groups. Ketamine intervention groups received 50 mg/kg/day ketamine for 8 weeks; KET + EX underwent 5 MICT sessions/week at 60-75% VO2max for 8 weeks post-withdrawal. Post-sampling of cerebral cortex, we evaluated histological changes, apoptotic cell numbers, Bax, Bcl-2, Caspase-3 mRNA/protein, 8-oxo-2'-deoxyguanosine (OXO) expression, glutathione peroxidase (GPX) and glutathione reductase (GR) mRNA and other oxidative stress and antioxidant markers levels. Effect sizes (ES) were used to assess group differences.

resultsMICT significantly reduced apoptotic cells (ES = 14.24, p < 0.0001), decreased Bax and caspase-3 protein expression, and increased Bcl-2 compared to the KET group (Bax: ES = 2.77, p = 0.005; caspase-3: ES = 7.73, p < 0.0001; Bcl-2: ES = 12.11, p < 0.001). It also lowered Bax and caspase-3 mRNA (Bax: ES = 4, p = 0.014; caspase-3: ES = 2.29, p = 0.024). MICT reduced OXO and increased GR and GPX mRNA and nitric oxide (NO) level (GR: ES = 2.02, p = 0.016; GPX: ES = 1.98, p = 0.035; OXO: ES = 11.39, p < 0.0001; NO: ES = 3.52, p = 0.003). Levels of malondialdehyde, myeloperoxidase, glutathione, superoxide dismutase, and catalase remained unchanged between groups.

conclusionMICT seems effective in reducing apoptosis and oxidative damage in the cerebral cortex of rats with long-term ketamine abuse.

Indexed as

ApoptosisCerebral CortexKetaminePhysical Conditioning, AnimalSubstance-Related DisordersAnimalsbcl-2-Associated X ProteinCaspase 3Glutathione PeroxidaseGlutathione ReductaseMaleOxidative StressProto-Oncogene Proteins c-bcl-2RatsRats, Wistarbcl-2-Associated X ProteinCaspase 3Glutathione PeroxidaseGlutathione ReductaseKetamineProto-Oncogene Proteins c-bcl-2addictionapoptosisdrug abuseexerciseketamineoxidative stress

Identifiers

PMID40062767
PMCPMC11892017

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